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Journal of Gastroenterology and Hepatology, ISSN 0815-9319, 03/2009, Volume 24, Issue 3, pp. 443 - 452
Background and Aims:  We examined extrinsic and intrinsic (endogenous) mitochondrial apoptosis pathways in experimental non‐alcoholic steatohepatitis (NASH).... 
mitochondria | methionine and choline deficiency | insulin‐like growth factor‐1 | TRAIL‐R killer/DR5 | TNF receptors | cell death pathways | p53 | Cell death pathways | TRAIL-R killer/DR5 | Methionine and choline deficiency | Mitochondria | Insulin-like growth factor-1 | P53 | HEPATOCYTE APOPTOSIS | ACIDS | DR5 | insulin-like growth factor-1 | NONALCOHOLIC STEATOHEPATITIS | LIVER-DISEASE | PATHOGENESIS | NECROSIS | TNF-ALPHA | LIGAND | GASTROENTEROLOGY & HEPATOLOGY | TRAIL-R killer | NF-KAPPA-B | HEPATIC STEATOSIS | Liver - pathology | Liver - enzymology | Fatty Liver - pathology | Mitochondria, Liver - metabolism | Caspase 3 - metabolism | Choline Deficiency - complications | Male | Alanine Transaminase - blood | Receptors, TNF-Related Apoptosis-Inducing Ligand - metabolism | Receptors, Tumor Necrosis Factor, Type I - metabolism | RNA, Messenger - metabolism | fas Receptor - metabolism | Tumor Suppressor Protein p53 - genetics | Time Factors | Receptors, Tumor Necrosis Factor, Type II - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Nutritional Status | Receptors, TNF-Related Apoptosis-Inducing Ligand - genetics | BH3 Interacting Domain Death Agonist Protein - metabolism | Disease Models, Animal | Methionine - deficiency | Receptors, Tumor Necrosis Factor - metabolism | Fatty Liver - metabolism | Mitochondria, Liver - pathology | Liver - metabolism | Mice, Inbred C57BL | Gene Expression Regulation | Tumor Suppressor Protein p53 - metabolism | Mitochondria, Liver - enzymology | Animals | Mice | bcl-X Protein - metabolism | Insulin-Like Growth Factor I - metabolism | Apoptosis | Fatty Liver - etiology | BH3 Interacting Domain Death Agonist Protein, metabolism | Receptors, Tumor Necrosis Factor, Type II, metabolism | Fatty Liver, pathology | Mitochondria, Liver, metabolism | Receptors, Tumor Necrosis Factor, metabolism | Cyclin-Dependent Kinase Inhibitor p21, metabolism | Insulin-Like Growth Factor I, metabolism | Caspase 3, metabolism | Antigens, CD95, metabolism | RNA, Messenger, metabolism | Tumor Suppressor Protein p53, metabolism | Methionine, deficiency | Choline Deficiency, complications | Tumor Suppressor Protein p53, genetics | bcl-X Protein, metabolism | Mitochondria, Liver, pathology | Liver, pathology | Alanine Transaminase, blood | Liver, metabolism | Fatty Liver, metabolism | Receptors, TNF-Related Apoptosis-Inducing Ligand, metabolism | Liver, enzymology | Fatty Liver, etiology | Mitochondria, Liver, enzymology | Receptors, Tumor Necrosis Factor, Type I, metabolism | Receptors, TNF-Related Apoptosis-Inducing Ligand, genetics | Messenger RNA | Choline | Methionine | Mitochondrial DNA | Tumor proteins | Peptide hormones | Growth factors
Journal Article
Journal Article
Biomaterials, ISSN 0142-9612, 2011, Volume 32, Issue 23, pp. 5438 - 5458
Abstract Oxidative stress is a major component of harmful cascades activated in neurodegenerative disorders. We sought to elucidate possible effects of... 
Advanced Basic Science | Dentistry | Oxidative stress | Mitochondria | Caspase-dependent apoptosis | Endoplasmic reticulum | Alginate oligosaccharide | PC12 cells | LOCALIZATION | ACTIVATION | MATERIALS SCIENCE, BIOMATERIALS | ENGINEERING, BIOMEDICAL | STABILIZATION | CHAPERONE | APOPTOSOME | CA2 | BAX | CYTOCHROME-C RELEASE | PROTEINS | MEMBRANE PERMEABILIZATION | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Calcium - metabolism | Glutathione - metabolism | Amyloid beta-Peptides - pharmacology | Oxidative Stress - physiology | Caspase 3 - metabolism | Endoplasmic Reticulum - metabolism | NF-kappa B - metabolism | Neurons - cytology | Peptide Fragments - pharmacology | Extracellular Signal-Regulated MAP Kinases - metabolism | PC12 Cells | Oligosaccharides - pharmacology | Proto-Oncogene Proteins c-bcl-2 - metabolism | Apoptosis Inducing Factor - pharmacology | Cell Nucleus - metabolism | Endoplasmic Reticulum - drug effects | Oxidation-Reduction - drug effects | Neurons - metabolism | Phosphorylation - drug effects | Glucuronic Acid - chemistry | Neurons - drug effects | Polysaccharide-Lyases - chemistry | Apoptosis Inducing Factor - metabolism | Cell Survival - drug effects | Cytochromes c - metabolism | Hydrogen Peroxide - pharmacology | Tumor Suppressor Protein p53 - metabolism | bcl-2-Associated X Protein - metabolism | Rats | Mitochondria - metabolism | Caspase 12 - metabolism | Hexuronic Acids - chemistry | Mitochondria - drug effects | HSP70 Heat-Shock Proteins - metabolism | Cell Shape - drug effects | Poly(ADP-ribose) Polymerases - metabolism | Animals | Models, Biological | Alginates - chemistry | NF-E2-Related Factor 2 - metabolism | HSP90 Heat-Shock Proteins - metabolism | Apoptosis - physiology | Oxidative Stress - drug effects | Cell Nucleus - drug effects | Neurosciences | Nervous system diseases | Biological products | Hydrogen peroxide | Heat shock proteins | Nerve growth factor | Superoxide | Mitochondrial DNA | Biochemistry | Antioxidants | Tumor proteins | Protein kinases | Alzheimer's disease | Apoptosis | Stresses | Surgical implants | Biomedical materials | Cell death | Cascades | Blocking | Activation | Kinases
Journal Article
Laboratory investigation, ISSN 1530-0307, 2012, Volume 92, Issue 5, pp. 713 - 723
Non-alcoholic steatohepatitis (NASH) is typically associated with pro-apoptotic caspase activation. A potential role for pro-inflammatory caspases remains... 
Inflammasome | Inflammation | Caspases | Non-alcoholic fatty liver disease | Non-alcoholic steatohepatitis | Fibrosis | MEDICINE, RESEARCH & EXPERIMENTAL | POPULATION | APOPTOSIS | non-alcoholic fatty liver disease | MICE DEFICIENT | FATTY LIVER-DISEASE | INJURY | NONALCOHOLIC STEATOHEPATITIS | MODEL | PATHOLOGY | inflammation | inflammasome | fibrosis | caspases | HEPATIC STEATOSIS | non-alcoholic steatohepatitis | Tumor Necrosis Factor-alpha - metabolism | Liver - pathology | Clodronic Acid - pharmacology | Fatty Liver - pathology | Actins - metabolism | Caspase 3 - metabolism | Hepatic Stellate Cells - metabolism | Caspase 1 - metabolism | Choline Deficiency - complications | Hepatocytes - pathology | Hepatocytes - metabolism | Fatty Liver - chemically induced | LIM Domain Proteins - metabolism | Liver Cirrhosis - chemically induced | Inflammation - metabolism | Caspase 3 - blood | Interleukin-1beta - metabolism | Choline Deficiency - metabolism | Liver Cirrhosis - metabolism | Muscle Proteins - metabolism | Antigens, Differentiation - metabolism | Kupffer Cells - metabolism | Hepatic Stellate Cells - pathology | Methionine - deficiency | Collagen Type I - metabolism | Fatty Liver - metabolism | Liver - metabolism | Mice, Inbred C57BL | Nuclear Proteins - metabolism | Choline Deficiency - pathology | Kupffer Cells - drug effects | Mice, Knockout | Animals | Caspase 1 - genetics | Caspase 1 - deficiency | Liver Cirrhosis - pathology | Mice | Transforming Growth Factor beta - metabolism | Nonalcoholic fatty liver disease (NAFLD) | nonalcoholic steatohepatitis (NASH)
Journal Article
Molecular and cellular biology, ISSN 0270-7306, 2003, Volume 23, Issue 4, pp. 1428 - 1440
Journal Article
PloS one, ISSN 1932-6203, 2015, Volume 10, Issue 6, pp. e0130624 - e0130624
Neuroinflammation is the local reaction of the brain to infection, trauma, toxic molecules or protein aggregates. The brain resident macrophages, microglia,... 
INTERLEUKIN-1 | ACTIVATION | MOLECULAR PLATFORM | INHIBITION | DISTINCT PATHWAYS | NEUROINFLAMMATION | MULTIDISCIPLINARY SCIENCES | IL-1-BETA | MECHANISMS | RECEPTORS | NALP3 INFLAMMASOME | Microglia - metabolism | Inflammasomes - metabolism | NLR Family, Pyrin Domain-Containing 3 Protein | Peptide Fragments - toxicity | Caspase 1 - metabolism | Interleukin-1alpha - metabolism | alpha-Synuclein - pharmacology | Interleukin-1beta - metabolism | Interleukin-1beta - secretion | Microglia - cytology | Brain - cytology | Interleukin-1beta - analysis | Enzyme-Linked Immunosorbent Assay | Microglia - drug effects | Amyloid beta-Peptides - toxicity | Mice, Inbred C57BL | Cells, Cultured | Mice, Knockout | Carrier Proteins - genetics | Animals | Carrier Proteins - metabolism | Caspase 1 - genetics | Caspase 1 - deficiency | Receptors, Purinergic P2X7 - metabolism | Mice | Interleukin-18 - metabolism | Astrocytes - metabolism | Cytokines | Health aspects | Nervous system diseases | Brain | Cell culture | Traumatic brain injury | Peptides | Aluminum sulfate | Homeostasis | Nervous system | Activation | Macrophages | Synuclein | Proteins | Rodents | Amyloid | Life sciences | Communication | Immune system | Neurodegenerative diseases | Astrocytes | Inflammation | Trauma | Molecular chains | Microglia | Interleukin 18 | Mode of action | Neurological diseases | Nigericin | Brain research | Ligands | Alum | Laboratory animals | Alzheimers disease | Chemokines | Index Medicus
Journal Article
Nature (London), ISSN 1476-4687, 2011, Volume 471, Issue 7340, pp. 637 - 641
Journal Article
The Journal of immunology (1950), ISSN 1550-6606, 2013, Volume 190, Issue 9, pp. 4640 - 4649
Dendritic cells (DC) are professional APCs that regulate innate and adaptive immunity. The role of fatty-acid synthesis in DC development and function is... 
CANCER-CELLS | APOPTOSIS | KAPPA-B ACTIVATION | UNFOLDED PROTEIN RESPONSE | CYTOKINE PRODUCTION | SYNTHASE INHIBITION | ER STRESS | MAP KINASE | MACROPHAGES | ENDOPLASMIC-RETICULUM STRESS | IMMUNOLOGY | Fatty Acids - immunology | Leukocytes, Mononuclear - metabolism | Chemokine CCL2 - immunology | Dendritic Cells - immunology | Humans | Caspase 3 - metabolism | Male | Cyclin B1 - metabolism | Interferon-gamma - metabolism | PPAR gamma - metabolism | CD4-Positive T-Lymphocytes - immunology | Mitogen-Activated Protein Kinase Kinases - metabolism | Liver - immunology | CD8-Positive T-Lymphocytes - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Liver - metabolism | CD4-Positive T-Lymphocytes - metabolism | Interleukin-12 - metabolism | B7-2 Antigen - metabolism | Cell Differentiation - immunology | Intercellular Adhesion Molecule-1 - metabolism | Proto-Oncogene Proteins c-akt - immunology | T-Lymphocytes, Cytotoxic - metabolism | Endoplasmic Reticulum - immunology | Interleukin-12 - immunology | Mice | Killer Cells, Natural - metabolism | CD8-Positive T-Lymphocytes - immunology | bcl-X Protein - metabolism | Fatty Acids - biosynthesis | Mitogen-Activated Protein Kinase Kinases - immunology | Caspase 3 - immunology | Endoplasmic Reticulum - metabolism | Genes, MHC Class II - immunology | PPAR gamma - immunology | Cyclin B1 - immunology | Leukocytes, Mononuclear - immunology | bcl-X Protein - immunology | Killer Cells, Natural - immunology | Chemokine CCL2 - metabolism | B7-2 Antigen - immunology | Fatty Acids - metabolism | Dendritic Cells - metabolism | T-Lymphocytes, Cytotoxic - immunology | B7-1 Antigen - immunology | Intercellular Adhesion Molecule-1 - immunology | Mice, Inbred C57BL | B7-1 Antigen - metabolism | Animals | Apoptosis - immunology | Interferon-gamma - immunology | Dendritic Cells - cytology | Fatty-acid synthesis | ER stress | NK cells | T cells | Bone marrow dendritic cells
Journal Article
The Journal of clinical investigation, ISSN 0021-9738, 01/2008, Volume 118, Issue 1, pp. 79 - 88
Despite great interest in cancer chemoprevention, effective agents are few. Here we show that chloroquine, a drug that activates the stress-responsive Atm-p53... 
MEDICINE, RESEARCH & EXPERIMENTAL | BCL-X-L | SIGNALING PATHWAYS | INDUCED APOPTOSIS | PHOSPHORYLATION | ATM | AUTOPHAGY | CYTOCHROME-C RELEASE | MYC-INDUCED LYMPHOMAGENESIS | TRANSGENIC MICE | P53 | Apoptosis - drug effects | Humans | Apoptosis - genetics | Male | Autophagy - drug effects | Burkitt Lymphoma - pathology | Neoplasms, Experimental - pathology | Chloroquine - pharmacology | Cell Transformation, Neoplastic - genetics | Autophagy - genetics | B-Lymphocytes - pathology | B-Lymphocytes - metabolism | Protein-Serine-Threonine Kinases - metabolism | Fibroblasts - metabolism | Tumor Suppressor Proteins - metabolism | Embryo, Mammalian - pathology | Cell Cycle Proteins - metabolism | Neoplasms, Experimental - prevention & control | bcl-2-Associated X Protein - metabolism | Ataxia Telangiectasia Mutated Proteins | Fibroblasts - pathology | Ataxia Telangiectasia - pathology | Ataxia Telangiectasia - genetics | Mice | Proto-Oncogene Proteins c-myc - genetics | Neoplasms, Experimental - metabolism | bcl-2 Homologous Antagonist-Killer Protein - genetics | bcl-2 Homologous Antagonist-Killer Protein - metabolism | Embryo, Mammalian - metabolism | Tumor Suppressor Protein p53 - genetics | DNA-Binding Proteins - metabolism | Caspases - metabolism | Lysosomes - metabolism | Burkitt Lymphoma - prevention & control | Mice, Mutant Strains | Tumor Suppressor Proteins - genetics | Neoplasms, Experimental - genetics | Burkitt Lymphoma - genetics | Cell Cycle Proteins - genetics | Female | Lysosomes - pathology | Antirheumatic Agents - pharmacology | bcl-2-Associated X Protein - genetics | Antirheumatic Agents - therapeutic use | Ataxia Telangiectasia - prevention & control | Caspases - genetics | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | Tumor Suppressor Protein p53 - metabolism | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Burkitt Lymphoma - metabolism | Chloroquine - therapeutic use | Ataxia Telangiectasia - metabolism | DNA-Binding Proteins - genetics | Cell Transformation, Neoplastic - metabolism | Proto-Oncogene Proteins c-myc - metabolism | Animals | Cyclin-Dependent Kinase Inhibitor p16 - metabolism | Cell Transformation, Neoplastic - pathology | Prevention | Chloroquine | Lysosomes | Dosage and administration | Research | Drug therapy | Health aspects | Cancer
Journal Article
PloS one, ISSN 1932-6203, 04/2012, Volume 7, Issue 4, p. e36019
Yersinia outer protein J (YopJ) is a type III secretion system (T3SS) effector of pathogenic Yersinia (Yersinia pestis, Yersinia enterocolitica and Yersinia... 
INDUCED CELL-DEATH | PROINFLAMMATORY CYTOKINE | LEGIONELLA-PNEUMOPHILA | DENDRITIC CELLS | BACTERIA-FACED MACROPHAGES | CHROMATIN PROTEIN HMGB1 | MULTIDISCIPLINARY SCIENCES | NLRP3 INFLAMMASOME | NF-KAPPA-B | III SECRETION SYSTEM | NALP3 INFLAMMASOME | Caspase 7 - metabolism | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Caspase 3 - metabolism | Caspase 1 - metabolism | Yersinia - pathogenicity | Interleukin-1beta - metabolism | HMGB1 Protein - metabolism | bcl-2-Associated X Protein - deficiency | Macrophages - microbiology | Yersinia pestis - metabolism | Yersinia Infections - pathology | Yersinia enterocolitica - pathogenicity | Yersinia Infections - microbiology | bcl-2-Associated X Protein - metabolism | Cathepsin B - metabolism | Caspase Inhibitors | Mice, Knockout | Macrophages - metabolism | Yersinia pseudotuberculosis - metabolism | Caspase 1 - deficiency | Yersinia enterocolitica - metabolism | Mice | Enzyme Activation | Yersinia pseudotuberculosis - pathogenicity | bcl-2 Homologous Antagonist-Killer Protein - deficiency | Caspase 8 - metabolism | bcl-2 Homologous Antagonist-Killer Protein - genetics | GTPase-Activating Proteins - metabolism | bcl-2 Homologous Antagonist-Killer Protein - metabolism | Necrosis - pathology | Yersinia Infections - metabolism | Protease Inhibitors - pharmacology | Protein Isoforms - metabolism | Female | Yersinia pestis - pathogenicity | bcl-2-Associated X Protein - genetics | GTPase-Activating Proteins - antagonists & inhibitors | Mice, Inbred C57BL | Bacterial Proteins - genetics | Cells, Cultured | Yersinia - metabolism | Cathepsin B - antagonists & inhibitors | Necrosis - metabolism | Mitochondria - metabolism | Immunity, Innate | Animals | Caspase 1 - genetics | Protein Binding | Bacterial Proteins - metabolism | Protein Isoforms - genetics | Cathepsins | Disease susceptibility | Interleukins | Macrophages | Necrosis | Apoptosis | Salmonella | Oxidative stress | Reactive oxygen species | Microscopic analysis | Bax protein | Bcl-2 protein | Toxicity | Downstream effects | Interleukin | Cytotoxicity | Homology | Infections | Activation | Kinases | HMGB1 protein | Caspase-3 | Caspase-1 | Pseudotuberculosis | Signal transduction | Mitochondria | Cell activation | Ribose | Cathepsin B | Stress response | Pathogens | Oxygen | Cell survival | Cytokines | Mortality | Poly(ADP-ribose) polymerase | Caspase | Adenosine diphosphate | IL-1β | Metabolism | Gene expression | Lymphoma | Caspase-8 | High mobility group proteins | Infectious diseases | Inhibitors | Lymphocytes B | Cell death | Isoforms | B-cell lymphoma
Journal Article